ABSTRACT
We have investigated the effect of inhaled adenosine on bronchomotor tone in 16 healthy and 24 allergic and non-allergic bronchopathic subjects. We determined the inhaled adenosine dose-response curves after no treatment and after treatment with aminophylline (240 mg in 10 min), reproterol (90 mcg in 2 min) and salbutamol (100 mcg in 2 min) administered intravenously 15 min before adenosine and reproterol (500 mcg) and salbutamol (200 mcg) administered by inhalation from a metered aerosol 30 min before adenosine on separate days. Without prior treatment, inhaled adenosine caused bronchoconstriction in both groups of subjects (normal, and atopic and non-atopic asthmatic ones), but the peripheral airways revealed only a moderate change in normal subjects. Aminophylline caused a greater inhibition of adenosine bronchoconstriction than did reproterol. These results suggest that inhaled adenosine bronchoconstriction involved purinergic transmission and that it is mediated via a P1/Ri (A-1/R1) receptor. Aminophylline is a potent antagonist at purinoceptor level. Reproterol inhibits bronchoconstriction by a mechanism independent of its effect on beta-adrenergic receptors. Because salbutamol, i.e. a beta 2-agonist bronchodilator, did not inhibit adenosine-induced bronchoconstriction (or very nearly so), our results support the view that reproterol antagonizes P1/Ri (A1/R1) tracheobronchial receptors.
Subject(s)
Bronchi/physiology , Receptors, Purinergic/physiology , Trachea/physiology , Adenosine/pharmacology , Adolescent , Adult , Aged , Albuterol/pharmacology , Aminophylline/pharmacology , Asthma/physiopathology , Bronchi/drug effects , Bronchitis/physiopathology , Bronchodilator Agents/pharmacology , Child , Drug Combinations , Female , Forced Expiratory Volume , Humans , Male , Metaproterenol/analogs & derivatives , Metaproterenol/pharmacology , Middle Aged , Receptors, Purinergic/drug effects , Theophylline/analogs & derivatives , Theophylline/pharmacology , Trachea/drug effectsABSTRACT
The present experiments evaluated in rats the effects of prenatal and postnatal exposure to a non-steroidal antiinflammatory agent, flunoxaprofen (5-10 and 20 mg/kg/day by the oral route), on cardiovascular function in the pups. In both conscious and anaesthetized rats pre- and postnatal flunoxaprofen exposure at the 30th and 60th day of age, significantly (P less than .05) induced a decrease of pressor response to carotid-sinus baroreceptor stimulation and to L-noradrenaline (0.1-1 and 5 micrograms/kg iv), and an increase of the hypotensive responses to L-isoprenaline (0.01-0.1 and 1 microgram/kg iv) and acetylcholine (0.01-0.1 and 1 microgram/kg iv). These effects were not observed in rats on the 90th day of age. Moreover, pre- and postnatal flunoxaprofen exposure did not modify systolic arterial blood pressure of plasma levels of catecholamines and acetylcholinesterases. Our results also show that in normotensive rats flunoxaprofen exposure during pregnancy did not affect the body weight, systolic or diastolic blood pressure or heart rate of pregnant rats. It did not affect the length of gestation, number of pups per litter or pup body weight. No macroscopic teratogenic effects were observed.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Benzoxazoles/pharmacology , Hemodynamics/drug effects , Prenatal Exposure Delayed Effects , Acetylcholine/pharmacology , Acetylcholinesterase/blood , Animals , Animals, Newborn , Anti-Inflammatory Agents, Non-Steroidal/blood , Benzoxazoles/blood , Blood Pressure/drug effects , Body Weight/drug effects , Catecholamines/blood , Catecholamines/pharmacology , Female , Heart Rate/drug effects , Isoproterenol/pharmacology , Male , Pregnancy , RatsABSTRACT
Pregnant female rats were exposed to antimony trichloride (0.1 and 1 mg/dl in their drinking water ad libitum) from the first day of pregnancy until weaning (22nd day after delivery). Pups were exposed to antimony trichloride (0.1 and 1 mg/dl in their drinking water ad libitum) from 22nd until 60th day of age. Antimony exposure did not significantly affect maternal and pup systolic arterial blood pressure, length of gestation, and number of newborn per litter. Antimony exposure decreased maternal and pup body weight. No macroscopic teratogenic effects have been observed. Whether or not pups were exposed to antimony trichloride, pressor responses to carotid occlusion and 1-noradrenaline and hypotensive responses to 1-isoprenaline and acetylcholine were significantly higher on the 60th than on the 30th day of age. In pups, prenatal and postnatal antimony exposure did not affect pressor response to carotidal occlusion, while it decreased pressor response to 1-noradrenaline and hypotensive response to 1-isoprenaline on the 60th day after birth. At last, antimony exposure at higher concentration decreased pup hypotensive response to acetylcholine on the 60th day.
